AIM:To explore the mechanism of pigment epithelium-derived factor(PEDF)in the development of experimental rat corneal neovascularization(CNV).

METHODS: Rat corneal alkaline burn model was established in both eyes by routine method in 40 anesthetized female Sprague-Dawley rats. The rats were randomly assigned to 2 groups with 20 rats each for topical administration of recombinant PEDF combined with chloramphenicol or normal saline combined with chloramphenicol(as control). At different intervals(4, 7, 10, and 14 days)of the treatment, rats were euthanized and the corneas removed for immunohistochemistry analyses to measure expression levels of PEDF, vascular endothelial growth factor(VEGF), Fas and FasL. The eyes of ten healthy rats were used as normal control. Meanwhile, the apoptosis of neovascular endothelial cells was detected by TUNEL method on the 4^th, 7^th, 10^th and 14^th day respectively after the burn.

RESULTS: There were high levels of PEDF expression and low levels of VEGF, Fas and FasL in the normal cornea. VEGF levels were significantly induced by chemical cauterization in the groups treated with chloramphenicol combined with normal saline, demonstrating CNV. In contrast, the PEDF treatment prevented the over expression of VEGF induced by the cauterization and unregulated the expression of Fas and FasL. In CNV tissues, the positive immune reaction of VEGF was most apparent during the 7^th day and then declined thereafter. However, the most positive expression of PEDF, Fas, FasL was on the 10^th day and then declined slowly after thereafter. The ratio of PEDF/VEGF raised from <1 to >1 in the course and the hinge was on the 10^th day. Certain time correlation existed between the dynamic expressions of VEGF and PEDF and the development of CNV. The expression of Fas and FasL correlated to PEDF closely in the whole procession which may underlie a simulative relationship between them. The apoptosis of CNV endothelial cells expressed most positively on the 10^th day and it was always much more intense in the PEDF group than in the normal saline group.

CONCLUSION: The expressions of VEGF and PEDF are remarkably expressed in experimental rat CNV tissues, and the fluctuation of which is consistent with the development of CNV. The breakdown of the balance between the two factors may play a role in CNV occurrence and development. That the PEDF downregulates VEGF expression and upregulates Fas and FasL expression which induces the apoptosis of CNV endothelial cells results in the inhibition of corneal NV induced by chemical cauterization. The results suggested the possible mechanism of PEDF in the therapeutic function for CNV diseases.